Improved outcomes for inborn babies with uncomplicated gastroschisis.

INTRODUCTION: Gastroschisis (GS) is a common abdominal wall defect necessitating neonatal surgery and intensive care. We hypothesized that inborn patients had improved outcomes compared to patients born at an outside hospital (outborn) and transferred for definitive treatment. METHODS: A single center, retrospective chart review at a pediatric tertiary care center was performed from 2010 to 2015. All patients whose primary surgical treatment of GS was performed at this center were included. We compared patients delivered within our center (inborn) to patients delivered outside of our center and transferred for surgical care (outborn). Babies with complicated gastroschisis were excluded. RESULTS: During the study period 79 patients with GS were identified. Of these, 53 were inborn and 26 were outborn. Sixteen patients were excluded for complicated GS. The rate of complicated GS was higher in the outborn group (32%) compared to the inborn population (11%) (p=0.03). Duration of stay, readmission rate and time on TPN were all significantly decreased for inborn patients, while time to definitive closure was similar. Mortality was 0% for both inborn and outborn patients. CONCLUSION: Patients with uncomplicated GS seem to benefit from delivery with immediate pediatric surgical care available eliminating the need for transfer. LEVEL OF EVIDENCE: III.

Dynamic retention: a technique for closure of the complex abdomen in critically ill patients.

Management of the open abdomen in the setting of massive visceral swelling or extensive intra-abdominal abscess may pose an extremely difficult surgical scenario. We herein describe the technique and results of dynamic-retention sutures used in 13 patients with abdominal catastrophes after trauma, vascular reconstruction, tumor extirpation, and intra-abdominal infection. Three of these patients died during their acute care hospitalization. The remaining 10 patients were discharged to home with no resultant fistulas and 1 recurrent hernia (10%). Dynamic-retention sutures provide a useful technique for the closure of the complex surgical abdomen. We observed a low complication rate. In properly selected patients, this technique avoids the use of mesh or additional surgical procedures such as skin grafting or plastic surgical reconstruction of the abdominal wall.

Ethanol inhibits mitogen activated protein kinase activity and growth of vascular smooth muscle cells in vitro.

The aim of this study was to determine the effect of ethanol on vascular smooth muscle cell proliferation and mitogen activated protein kinase (MAPK) signaling. Rat aortic smooth muscle cell growth in vitro was determined by measuring cell counts and [3H]thymidine incorporation. MAPK signaling was determined by assessing MEK (also referred to as MAPK kinase) activity by measuring phosphorylated extracellular signal-regulated kinase (pp44ERK - 1 and pp42ERK - 2) expression, and ERK activity by measuring ERK-2-dependent phosphorylation of myelin basic protein (MBP). In quiesced smooth muscle cells, ethanol treatment (24 h) inhibited serum-stimulated mitogenesis in a dose-dependent manner, (IC50 = 60 mM), in the absence of any effect on smooth muscle cell viability. In addition, ethanol treatment caused a significant shift to the right in the smooth muscle cell growth curve, extending the population doubling time from approximately 48 h (control) to approximately 70 h (ethanol). Acute (15 min) ethanol treatment reduced serum-stimulated pp44ERK - 1 and pp42ERK - 2 expression in a dose dependent fashion; 24.5+/-1.5% and 77.6+/-3.2% inhibition for 20 mM and 160 mM ethanol, respectively. Furthermore, there was a significant dose-dependent decrease in ERK2 activity in ethanol treated smooth muscle cells as compared to control smooth muscle cells. These data demonstrate an inhibitory effect of ethanol on smooth muscle cell proliferation and MAPK signalling in vitro. It is tempting to speculate that these actions of ethanol may contribute to its cardiovascular effects in vivo.

Benign rectal ulcer: an underground cause of inpatient lower gastrointestinal bleeding.

BACKGROUND: Although it is uncommon, significant bleeding per rectum presents one of the most difficult emergency problems. Bleeding from a rectal ulcer is not well recognized as a cause of such bleeding. METHODS: From July 2000 through December 2000, 195 consecutive patients with significant blood loss per rectum were reviewed. RESULTS: Forty-eight cases in whom significant gastrointestinal (GI) bleeding occurred following prior hospitalization were identified. Sources of bleeding were gastroduodenal in 38 cases (79%) and colorectal in 10 cases (21%). The causes of inpatient colorectal bleeding were benign rectal ulcer (n = 4), ischemic colitis (n = 3), neoplasia (n = 2), and diversion colitis (n = 1). CONCLUSION: The differential diagnosis for inpatients who develop new inpatient GI bleeding differs from that of patients who develop outpatient GI bleeding. Careful examination of the rectum following rectal instrumentation is critical. In addition to the standard resuscitative measures, the identification and treatment of rectal ulcers in this group of patients is of paramount importance. The treatment options for bleeding rectal ulcer include conservative therapy, cauterization, embolization, banding, and local excision.

Gamma probe-confirmed laparoscopic accessory splenectomy.

The simultaneous occurrence of idiopathic thrombocytopenic purpura (ITP) and Hodgkin's disease in the same patient is uncommon. There have been only a limited number of reported cases of newly diagnosed ITP following Hodgkin's disease. Even more uncommon is the development of ITP after splenectomy for Hodgkin's disease. Of the reported cases of ITP following splenectomy for Hodgkin's disease, all have been successfully treated with medical therapy. We report an unusual case of an accessory spleen causing ITP in a patient who had undergone a splenectomy for Hodgkin's disease 10 years earlier. The patient underwent hand-held gamma-probe-assisted laparoscopic accessory splenectomy.

Management of massive retroperitoneal hemorrhage from an adrenal tumor.

Spontaneous massive retroperitoneal hemorrhage from an adrenal gland is a rare event. A thoughtful and meticulous approach to such a patient, with appropriate diagnostic studies, ICU and surgical care are essential for patient survival. In patients with active bleeding, angiographic embolization is a valuable adjunct to achieve hemostasis, to allow for further work-up of the adrenal tumor, and an improved subsequent oncologic resection. Hemodynamically unstable patients, however, may require supportive transfusions in the intensive care unit, potential embolization if deemed feasible, or urgent surgical exploration. If possible, however, the acute surgical removal of an adrenal tumor within a large retroperitoneal hematoma should be avoided, as under such conditions a proper oncologic resection may not be possible. The possibility of a pheochromocytoma must always be entertained. Early recognition and treatment of patients with presumed adrenal insufficiency may decrease patient morbidity and mortality.

Ethanol enhances basal and flow-stimulated nitric oxide synthase activity in vitro by activating an inhibitory guanine nucleotide binding protein.

The aim of this study was to determine the effect of ethanol on endothelial nitric oxide synthase (eNOS), the enzyme responsible for the production of the important vasoactive agent nitric oxide. The effect of ethanol (0.8-160 mM) on both basal and flow-stimulated eNOS activity was determined using cultured bovine aortic endothelial cells (EC). In "static" EC ethanol dose-dependently increased basal eNOS activity with a maximum response (approximately 2.0-fold increase) achieved at 40 mM in the absence of any effect on cell viability or nitric oxide synthase protein expression. Pertussis toxin (PTX) pretreatment significantly inhibited the ethanol-induced increase in basal eNOS activity. EC exposed to steady laminar flow exhibited a flow- and time-dependent increase in eNOS activity. Ethanol significantly enhanced the laminar flow-induced eNOS response from 0.62 +/- 0.1 to 1.06 +/- 0. 06 pmol [14C]citrulline/mg/min, a response that was inhibited by PTX. PTX-catalyzed ribosylation of Gialpha substrates, an index of G-protein functional activity, was increased in laminar flow-exposed EC compared with static controls and was further enhanced by ethanol treatment. Likewise, EC exposed to low ( approximately 0.5 dynes/cm2) and high ( approximately 12 dynes/cm2) pulsatile flow demonstrated increased eNOS activity, an effect that was associated with increased PTX-catalyzed ribosylation of Gialpha substrates. Ethanol enhanced the low flow response in a PTX-sensitive manner. These data demonstrate a stimulatory effect of ethanol on basal and flow-stimulated eNOS activity, mediated in part by a mechanism involving a PTX-sensitive G protein.

Preoperative terminal ileal and colonic resection histopathology predicts risk of pouchitis in patients after ileoanal pull-through procedure.

OBJECTIVE: This study seeks to compare the histopathology of preoperative terminal ileal and colonic resection specimens with pouch biopsies after the ileoanal pull-through (IAPT) procedure. SUMMARY BACKGROUND DATA: Pouchitis is the most frequent complication of transanal continent reservoirs in patients after IAPT. METHODS: The authors conducted 751 consecutive pouch biopsies on 73 patients with inflammatory bowel disease or familial adenomatous polyposis who underwent IAPT by a single surgeon over a 10-year period. In this preliminary report, a pathologist, in blinded fashion, has graded 468 of the IAPT pouch biopsies and 67 of the patients' preoperative terminal ileal and colonic resection histopathology to date. Colonic histopathology was graded by the extent and severity of disease, terminal ileal and pouch histopathology by active inflammation, chronic inflammation, lymphocyte aggregates, intraepithelial lymphocytes, eosinophils, and villous blunting. RESULTS: Extent of colonic disease (gross and microscopic) was a significant predictor of active inflammation in subsequent IAPT pouch biopsy specimens. Also, the gross extent of colonic disease exhibited a significant linear association with pouch inflammation. However, the severity of colonic disease was not significantly predictive of active inflammation in subsequent IAPT pouch biopsies. Terminal ileal active and chronic inflammation were significant predictors of subsequent IAPT pouch inflammation. Although lymphocyte aggregates and intraepithelial lymphocytes were not predictive, terminal ileum eosinophils and villous blunting were significant predictors of active inflammation in subsequent IAPT pouch biopsy specimens. CONCLUSIONS: Preoperative terminal ileal and colonic histopathology predicts active inflammation of pouches after IAPT. Patients who are preoperatively assessed to have extensive disease of the colon, ileal disease ("backwash ileitis"), or both appear to be at greater risk for the development of pouchitis after IAPT.

Ethanol inhibits basal and flow-induced vascular smooth muscle cell migration in vitro.

BACKGROUND: Alcohol consumption protects against coronary heart disease by as yet unclear mechanisms. The aim of this study was to determine the effect of ethanol on vascular smooth muscle cell (SMC) migration which plays an important role in the pathogenesis of atherosclerosis. MATERIALS AND METHODS: Cultures of human SMC under static (no flow) or pulsatile flow conditions (perfused transcapillary culture system) were pretreated in the absence or presence of ethanol (EtOH) whereupon their random migration (chemokinesis) was assessed by Transwell assay. RESULTS: Ethanol pretreatment (24 h) dose dependently inhibited migration of HuSMC from static cultures with a maximal inhibition of 60.8 +/- 4.4% observed at 40-80 mM, in the absence of any effect on cell adhesion or cell viability as assessed by trypan blue exclusion. In HuSMC exposed to pulsatile flow (0.3 to 25 ml/min, 24 h), there was a flow-dependent increase in migration ranging from a 1.3 +/- 0.16- to 2.67 +/- 0.26-fold increase, compared to static cells, concomitant with a significant increase in urokinase-type plasminogen activator (uPA) mRNA levels. Ethanol pretreatment (20-80 mM, 24 h) dose dependently inhibited the flow-induced increase in SMC migration but did not affect uPA mRNA expression. CONCLUSIONS: The inhibitory effect of ethanol on basal and flow-stimulated SMC migration may be relevant to its cardiovascular effects in vivo.

Sustained pulsatile flow regulates endothelial nitric oxide synthase and cyclooxygenase expression in co-cultured vascular endothelial and smooth muscle cells.

This study addresses the effect of sustained increased pulsatile flow on nitric oxide synthase (NOS) and cyclooxygenase (Cox) expression and activity in co-cultured endothelial cells (EC) and vascular smooth muscle cells (SMC). Using a perfused transcapillary co-culture system which permits the chronic exposure of cultured EC and SMC to physiological shear stresses, co-cultures were exposed to step-wise increases in flow up to: (i) 2 ml/min (low flow: 0.5 dyn/cm2): or (ii) 44 ml/min (high flow: 15 dyn/cm2) and maintained for 72 h before SMC and EC were harvested separately. There was no NOS activity or protein expression in co-cultured SMC under flow conditions. There was a significant increase in eNOS activity in co-cultured EC under high flow conditions, compared to low flow, which correlated with an increase in eNOS expression and mRNA levels. The flow-induced increase in eNOS activity was potentiated by indomethacin treatment, suggesting a modulatory role for a cyclooxygenase product. Prostacyclin levels in co-culture perfusate were significantly elevated under high flow conditions. While both co-cultured EC and SMC expressed cyclooxygenase (Cox-I and Cox-II), they were differentially regulated by pulsatile flow, EC Cox-I and Cox-II protein expression were both decreased. Indomethacin treatment increased the expression of both Cox-I and Cox-II in co-cultured SMC under high flow conditions. We conclude that sustained increases in pulsatile flow maintain elevated eNOS and Cox protein expression and activity in EC while decreasing Cox expression in co-cultured SMC. These data suggest that regulation of these pathways may contribute to flow-induced vascular remodeling in vivo.

Enhanced cyclooxygenase-1 expression within the superior mesenteric artery of portal hypertensive rats: role in the hyperdynamic circulation.

Portal hypertension (PHT) is characterized by splanchnic hyperemia due to enhanced production of vasodilator substances. Enhanced vasodilation and increased splanchnic blood flow contribute to the elevated portal pressure characteristic of PHT. The aim of this study was to determine whether cyclooxygenase (Cox) expression is altered in PHT vessels and whether chronic inhibition of this enzyme impacts on splanchnic blood flow in PHT. PHT was created in Sprague-Dawley rats by a partial portal vein ligation. Control animals were sham operated. Plasma 6-keto-PGF1alpha (prostaglandin F1alpha) levels were significantly elevated in PHT after 2 days as compared with sham and remained elevated up to day 15. Treatment with indomethacin (2 mg/kg i.p. daily for 15 days) resulted in a significant decrease in 6-keto-PGF1alpha levels, which was concomitant with a significant decrease in superior mesenteric artery blood flow (Qsma) after 15 days in PHT rats. Cox-I expression was differentially enhanced in the PHT superior mesenteric artery and thoracic aorta during the development and progression of PHT. In contrast, Cox-II messenger RNA (mRNA) and protein expression was not detected in either of these vessels throughout the development of PHT. These data suggest that PHT is associated with enhanced Cox-I expression within the splanchnic vasculature concomitant with elevated plasma prostacyclin levels and a significant pressor response to indomethacin in PHT animals. We conclude that enhanced Cox-I expression results in increased prostacyclin levels that partially contribute to the maintenance of the hyperemia typical of PHT.